Sorry about these questions! I've done by best to look them up on the internet - I think I've spent over two hours on each one of these but I haven't been able to come to a conclusive answer, since they conflict with my textbook...

Please answer these! I'm really struggling and yeah.. I would be prepared to pay for these questions to be answered - I've spent so much time (over a full day) searching for answers to these without success.. If you demand payment to answer these I will gladly give it (at a reasonable price.. I'm not able to work yet, so its my pocket money I've saved)

Drug design1. With rational drug design, is it true that there are two different types? (ligand-based and structure-based) These are the notes I have on it, but I would have thought that they are used together..

Endocrine system2. In a positive feedback system, a hormone produced can act on the gland that produced it, which stimulates more creation. They gave an example of the contractions during birth. If this is true, how does the process stop?

3. Auxins, at high concentrations, stimulate the elongation of cells a plant's stems, but at high concentrations, inhibit growth of roots. Do auxins have any special characteristics at low concentrations?

Infection and disease4. Exotoxins stay in the cell after the bacteria dies.. Don't all toxins stay anyway? Also, aren't exotoxins removed by the liver and kidneys, like endotoxins?

5. According to my textbook, prions can convert normal proteins into proteins simply by coming into contact with them. That must mean they're very infectious. My book goes and says that

It appears that we all contain the genetic instructions to make normal prion protein. The protein occurs mainly in nerve cells and its function is unknown. If we become infected with a defective prion it converts normal protein into prion protein.

Does this somehow indicate that there are "defective" and "non-defective" prions, and therefore mean that the above image is incorrect?

6. Wikipedia says that interferons are produced by lymphocytes, but my book seems to imply that they are produced by the (infected) cells themselves.Which is true?

7. With fungal spores, do spores germinate into sporeling, which then develop into bacteria?

8."Bacterial antibiotics do not act against fungi" - why not?

9. "antifungal ointments and oral preparations are used to treat fungal infections." - what is an oral preparation?

10. Examples of arthropods are nits, houseflies and mosquitoes. Are these correct?

Immune System11. The lungs have surfactants, which as opsonins (substances that targets an antigen for an immune response) - is this true?

12. Are macrophages and phagocytes nautral killer cells? Wikipedia says that "NK cells are activated in response to interferons or macrophage-derived cytokines", which would mean that macrophages are not? But my book suggests otherwise...

13. How are complement proteins activated? I don't really understand my book, which words it like so:

When infection occurs, antibody–antigen complexes form and these activate complement proteins. The activation of one kind of complement protein results in a cascade effect where each activated complement protein then activates another, and so on down the chain.

1. of course you can use both, but their are kind of complementary. In the first case you have database of millions of possible ligands and try them all on your protein. In the other case, you have structure of your protein and determines the minimum, which binds into it. Then you try different modifications.

2. there's usually some negative loop as well

3. they don't initiate the elongation of stems and do not inhibit elongation of roots

5. why would be that picture incorrect?

7. fungal spores do not develop into bacteria

8. Probably because biggest concurents of bacteria are other bacteria, not fungi